Vestibular dysfunction in migraine: effects of associated vertigo and motion sickness |
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Authors: | Seong-Hae Jeong Sun-Young Oh Hyo-Jung Kim Ja-Won Koo Ji Soo Kim |
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Institution: | (1) Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, 300 Gumi-dong, Bundang-gu, Seongnam-si, Gyeonggi-do, 463-707, South Korea;(2) Department of Neurology, Chungnam National University Hospital, Daejon, South Korea;(3) Department of Neurology, Chonbuk National University Hospital, Jeonju, South Korea;(4) Department of Otolaryngology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam-si, Gyeonggi-do, South Korea; |
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Abstract: | The mechanisms of vestibular migraine and motion sickness remain unknown. The aims of this study were to determine interictal
vestibular dysfunction in migraineurs according to associated dizziness/vertigo and motion sickness, and to find out whether
impaired uvulonodular inhibition over the vestibular system underlies the vestibular symptoms and signs by measuring tilt
suppression of the vestibulo-ocular reflex (VOR). One hundred and thirty-one patients with migraine 65 with vestibular migraine
(MV), 41 with migrainous dizziness (MD), and 25 with migraine only (MO)] and 50 normal controls underwent evaluation of vestibular
function. Motion sickness was assessed using the motion sickness susceptibility questionnaire (MSSQ) and subjective scale.
Compared with normal controls and MO group, patients with MV/MD showed increased VOR time constant (TC) and greater suppression
of the post-rotatory nystagmus with forward head tilt. The mean MSSQ score and subjective scale were highest in MV group,
followed by MD, MO, and controls (p = 0.002, p < 0.001). Multiple linear regression model analyses revealed that motion sickness is an independent factor of TC prolongation
(p = 0.024). Twenty-eight (21.4%) patients with migraine also showed perverted head shaking nystagmus and 12 (9.2%) had positional
nystagmus. In view of the increased tilt suppression of the VOR, we speculate that dysfunction of the nodulus/uvula may not
account for the prolonged TCs in MD/MV. Instead, innate hypersensitivity of the vestibular system may be an underlying mechanism
of motion sickness and increased TC in MD/MV. The increased tilt suppression may be an adaptive cerebellar mechanism to suppress
the hyperactive vestibular system in migraineurs. |
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